Influence of Insulin Resistance and Adipokines in the Grade of Steatosis of Nonalcoholic Fatty Liver Disease

The objective of this work was to study the influence of insulin resistance and adipokines on the grade of steatosis in patients with NAFLD (nonalcoholic fatty liver disease) diagnosed by liver biopsy. A sample of 24 NAFLD patients was analyzed in a cross-sectional study. All patients with a two-week weight-stabilization period before recruitment were enrolled. A liver biopsy was realized. Weight, basal glucose, insulin, insulin resistance (HOMA), total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides, and adipokines blood levels were measured. A nutritional evaluation (dietary intake, indirect calorimetry, and bioimpedance) was performed. The mean age was 41.6 ± 8.7 years and the mean body mass index (BMI) 29.4 ± 4.7. Twelve patients had a low grade of steatosis (grade 1 of the Brunt classification) and 12 patients had a high grade of steatosis (grade 2 or 3). Only HOMA was higher in patients with a high grade of steatosis (1.4 ± 0.5 vs. 2.8 ± 1.7 units; P < 0.05). Anthropometric data and dietary intake were similar for both groups. Blood levels of adiponectin were higher in patients with a low grade of steatosis (37.7 ± 22.5 vs. 24.2 ± 33 ng mL⁻¹; P < 0.05). Blood levels of resistin were higher in patients with a high grade of steatosis (2.36 ± 0.6 vs. 2.8 ± 0.6 mg mL⁻¹; P < 0.05), without differences in TNF-α or leptin levels. In logistic regression analysis, the HOMA-IR remained in the model, with an odds ratio to develop high grade of steatosis of 7.8 (95% CI: 1.8–75) with each 1 unit of HOMA-IR adjusted by age, sex, BMI, and dietary intake. This study demonstrates that insulin resistance determined with the HOMA model is associated with a high grade of steatosis in patients with NAFLD.     

Gallstone Disease Does Not Predict Liver Histology in Nonalcoholic Fatty Liver Disease

Background/Aims

We sought to examine whether the presence of gallstone disease (GD) in patients with biopsy-proven nonalcoholic fatty liver disease (NAFLD) is associated with liver fibrosis and histological nonalcoholic steatohepatitis (NASH) score.

Methods

We included 441 Turkish patients with biopsy-proven NAFLD. GD was diagnosed in the presence of sonographic evidence of gallstones, echogenic material within the gallbladder with constant shadowing and little or no visualization of the gallbladder or absence of gallbladder at ultrasonography, coupled with a history of cholecystectomy.

Results

Fifty-four patients (12.2%) had GD (GD+ subjects). Compared with the GD- subjects, GD+ patients were older, had a higher body mass index and were more likely to be female and have metabolic syndrome. However, GD+ patients did not have a higher risk of advanced fibrosis or definite NASH on histology. After adjustment for potential confounding variables, the prevalence of GD in NAFLD patients was not associated with significant fibrosis (≥2) (odds ratio [OR], 1.06; 95% confidence interval [CI], 0.53 to 2.21; p=0.68) or definite NASH (OR, 1.03; 95% CI, 0.495 to 2.12; p=0.84).

Conclusions

The presence of GD is not independently associated with advanced fibrosis and definite NASH in adult Turkish patients with biopsy-proven NAFLD.     

The Effects of Rosiglitazone,Metformin, and Diet with Exercise in Nonalcoholic Fatty Liver Disease

Our aım was to evaluate effects of metformin, rosiglitazone, and diet with exercise in nonalcoholic fatty liver disease. Forty-seven patients (mean age, 44±10 years; 17 female) whose ALT levels had been high for at least 6 months and with hepatosteatosis detected by liver biopsy and/or USG were enrolled in this study. Of these, 12 were treated with 850 mg/day metformin (group 1), 11 with 4 mg/day rosiglitazone (group 2), and 24 with diet and exercise (group 3) for 1 year. ALT normalization at months 6 and 12 was accepted as treatment response. Liver biopsy was performed in all patients in groups 1 and 2 before treatment and 12 patients (4 in group 1, 8 in group 2) after treatment; but in group 3 it was performed only in patients who approved this procedure (12 patients). Body mass index did not change in groups 1 and 2, but it decreased significantly in group 3 (30±3 to 28±2 kg/m²) at month 12. Treatment response rate was 33.3, 54.5, and 54.2% in groups 1, 2, and 3, respectively, at month 6. This rate was 22.2, 37.5, and 41.2 in groups 1, 2, and 3, respectively, at month 12. Rate of steatosis and stage of fibrosis did not change after treatment. Diet with exercise seems to be superior to metformin and rosiglitazone. Decreasing treatment response at month 12 compared to month 6 may be due to fluctuations of ALT levels. Treatment response should be evalulated histologically.     

Methylenetetrahydrofolate Reductase C677T Mutation and Nonalcoholic Fatty Liver Disease

A mutation in the methylenetetrahydrofolate reductase (MTHFR) gene is known as one of the causes of hyperhomocyteinemia. The oxidation products of homocysteine can initiate lipid peroxidation, which has a central role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). We aimed to assess the possible role of the MTHFR C677T mutation in the progression of simple steatosis to an advanced form of NAFLD. Thirty-four patients with NAFLD diagnosed by histologic analysis and 282 healthy controls were included in the study. The discrimination of nonalcoholic steatohepatitis (NASH) from another NAFLD was made by NAFLD activity score (NAS), and a NAS≥5 was considered NASH. Patients with either NASH or nonalcoholic fatty liver (NAFL) and controls were evaluated for frequency of the MTHFR C677T mutation. The frequency of the MTHFR C677T mutation was 53.5% (CT, 44.7%; TT, 8.9%) in controls and 41.5% (CT, 37.7%; TT, 3.8%) in patients (odds ratio [OR], 0.62; 95% confidence interval [CI], 0.34–1.12). There was no statistical difference in the frequency of this genotype between patients with NAFL and those with NASH (36% [CT, 28%; TT, 8%] vs 46.4% [CT, 46.4; TT, 0%]; OR, 0.65; 95% CI, 0.22–1.96). According to this study, the MTHFR C677T mutation does not seem to be a risk factor for the progression of NAFL to NASH.     

非酒精性脂肪肝患者血清抵抗素与胰岛素抵抗关系的研究

目的 探讨非酒精性脂肪肝患者血清抵抗素水平及其与肥胖、胰岛素抵抗、血糖、血脂的关系.方法 选择非酒精性脂肪肝患者100例,正常对照30例,采用ELISA方法测定空腹血清抵抗素,同时检测其身高、体重、腰围、臀嗣、血糖、血脂、肝功能及胰岛素水平,并计算体重指数、腰臀比和胰岛索敏感指数.结果 非酒精性脂肪肝患者血清抵抗素水平为17.68±5.2 ng.ml,高于正常对照组的12.85±4.4 ng.ml,P<0.01.相关分析显示,血清抵抗素与体重指数、甘油三酯呈正相关关系(分别为r=0.376、0.426,P<0.05),与胰岛素敏感指数呈负相关关系,(r=-0.584,P<0.01),而与腰臀比、总胆固醇、低密度酯蛋白胆固醇、高密度脂蛋白胆固醇、血糖无相关性,(P>0.05).结论 在非酒精性脂肪肝的发病过程中,抵抗素可能参与了胰岛素抵抗.     

Serum Lipid Abnormalities and Nonalcoholic Fatty Liver Disease in Adult Males

Background

Dyslipidemia is a risk factor for nonalcoholic fatty liver disease (NAFLD). The aim of our study was to determine the associations of serum lipid indexes with NAFLD in adult males.

Nonalcoholic Fatty Liver Disease: Dyslipidemia,Risk for Cardiovascular Complications,and Treatment Strategy

Studies have shown that nonalcoholic fatty liver disease (NAFLD) is strongly associated with several metabolic disorders and diseases, such as obesity, type 2 diabetes mellitus, and dyslipidemia. In NAFLD, dyslipidemia is manifested as increased serum triglyceride and low-density lipoprotein cholesterol levels and decreased high-density lipoprotein cholesterol levels, all of which are key risk factors for cardiovascular disease (CVD). CVD is a leading cause of mortality in NAFLD patients. Thus, implementation of an aggressive therapeutic strategy for dyslipidemia with hypolipidemic agents may mitigate the risk for CVD among NAFLD patients. Here, we provide a current review of literature regarding NAFLD, with particular emphasis on dyslipidemia and available treatment options.     

Ideal Cardiovascular Health Is Inversely Associated with Nonalcoholic Fatty Liver Disease: A Prospective Analysis

Background

Cardiovascular health has been proven to be associated with major cardiometabolic diseases. However, little is known of associations between cardiovascular health and nonalcoholic fatty liver disease.

The Impact of Nonalcoholic Fatty Liver Disease in Primary Care: A Population Health Perspective

Nonalcoholic fatty liver disease (NAFLD) is the leading cause of liver disease worldwide, with rising rates in parallel to those of obesity, type 2 diabetes, and metabolic syndrome. NAFLD encompasses a wide spectrum of pathology from simple steatosis to nonalcoholic steatohepatitis (NASH) and cirrhosis, which are linked to poor outcomes. Studies confirm a significant amount of undiagnosed NAFLD and related fibrosis within the community, increasing the overall burden of the disease. NAFLD appears to be more prevalent in certain populations, such as those with type 2 diabetes and metabolic syndrome. Early detection and lifestyle modifications, including weight loss and regular exercise, have been shown to improve outcomes. Adverse cardiovascular events are a key contributor to NAFLD-associated morbidity and mortality, and efforts to minimize their occurrence are essential. A targeted and algorithmic approach using noninvasive diagnostic techniques is promptly required to identify and risk-stratify patients with NAFLD. Patients at low risk of progression to NASH and advanced fibrosis can be managed in the primary care setting, while those at high risk of disease progression should be referred to hepatology specialists for surveillance and treatment. This review summarizes the key data of NAFLD's impact within primary care populations and proposes a potential algorithmic approach to identifying and managing such patients.     

非酒精性脂肪肝与高尿酸血症的关系

目的了解非酒精性脂肪肝（NAFLD）与高尿酸血症（HUA）间的相互关系,进一步证实其隐性危害。方法从本校2010年9月-2011年5月体检者中,优选符合标准9050例为本研究对象,其中男性4655例,女性4395例,年龄在24～85岁之间;以超声诊断为基础,将受检者分为两组,即NAFLD组和无NAFLD组,同时检查血中尿酸水平。结果NAFLD组1875例中有462例伴有高尿酸血症（24．6％）,无NAFLD组7175例中检测到尿酸升高者633例（8．8％）,两组比较具有统计学差异（P〈0．001）。结论NAFLD组与血清尿酸浓度有密切关系,提示高尿酸血症是NAFLD发生和发展中的危险因素。     

原发性高血压患者合并脂肪肝与动脉粥样硬化的关系

目的:探讨原发性高血压患者非酒精性脂肪肝与颈动脉粥样硬化及冠心病发病的相关性。方法:入选原发性高血压患者66例,按是否合并脂肪肝分组(脂肪肝组37例,非脂肪肝组29例)。记录所有患者的血压、体重指数、生化指标、颈动脉B超和冠状动脉造影结果。结果:两组的年龄、性别、高血压病程、血压水平相近(P>0.05),血总胆固醇、高密度脂蛋白、尿酸、尿微量白蛋白无显著差异(P>0.05)。脂肪肝组的空腹血糖、甘油三脂、体重指数高于非脂肪肝组(P<0.05),颈动脉内膜中层厚度显著增加(1.13±0.25 vs 0.96±0.24mm;P<0.01)。颈动脉斑块及冠心病发生率在脂肪肝组显著增加(P<0.05),脂肪肝组冠心病患者的血管病变重于非脂肪肝组冠心病患者(P<0.05)。结论:合并脂肪肝的原发性高血压患者更易发生颈动脉粥样硬化,且冠心病发病率增加,提示脂肪肝的并存增加原发性高血压患者动脉粥样硬化疾病的风险。